-------
Aquatic plants are very sensitive to atrazine. Algal photosynthe-
sis and growth were inhibited by 50% at levels ranging from 0.1 to 5.0
ppm during a 3-hour exposure period (Stratton, 1984). Veber et al.
(1981) noted a marked inhibitory effect on algal growth during a 7-day
exposure at levels ranging from 0.5 to 2.5 ppm; however, there was
recovery at lower concentrations. At 25 ppm atrazine inhibited growth
greater than 50% in thirty-six species of algae during a 2-week expo-
sure period (O'Kelly and Deason, 1976). Growth of two species was
inhibited greater than 50% at 0.001 ppm atrazine in the same study.
Stratton (1981) found the EC50 value for photosynthesis and growth for
green and bluegreen algae to range from 0.03 to 4 ppm and noted that
atrazine was more toxic than any of its metabolites. Photosynthetic
150 (50 percent inhibition) values for four species of aquatic vascu-
lar plants ranged from 0.077 to 0.104 ppm after a 2-hour exposure
period (Jones and Winchell, 1984). Growth 150 values for aquatic
vascular plants ranged from 0.08 to 1.104 ppm during a 3- to 6-week
exposure period (Forney and Davis, 1981).
Toxicity experiments with model ecosystems have shown that aquatic
plants and benthic organisms are directly affected by atrazine. Atra-
zine applied to artificial streams at 1 and 10 ppm severely inhibited
growth of algae and decreased biomass at both exposure levels
(Kosinski, 1984). Atrazine applied to estuarine microcosms at 0.13
ppb significantly decreased photosynthetic oxygen production by
Potamogeton perfoliatus immediately following treatment; however, the
plants recovered within 2 weeks, even though atrazine levels remained
constant. A higher concentration (1.2 ppb) of atrazine significantly
decreased photosynthetic oxygen production by P. perfoliatus which did
not recover during the 4-week exposure period (Cunningham et al.,
1984). Atrazine was applied at concentration levels ranging from 2.0
to 6.0 ppm to ponds, and found to be toxic to several species of
aquatic plants and benthic organisms. Benthic organisms which were
most sensitive included mayflies, caddisflies, leeches, and gastropods
(Walker, 1964). Microcosm experiments also showed that atrazine can
cause indirect effects on aquatic organisms and changes in species
composition (deNoyelles et al., 1982). Applied at 20 and 500 ppm to
pond ecosystems, atrazine decreased phytoplankton growth, but more
resistent species eventually became reestablished during the 136-day
experiment. Decreased phytoplankton growth, however, caused indirect
effects on growth and reproduction of zooplankton.
Bioaccumulation of atrazine in aquatic animals does not appear to
be a major concern in comparison to other pesticides. Aquatic
invertebrates, limpets, and waterfleas had bioconcentration factors of
3-4 and 1-10, respectively (Gunkel and Streit, 1980; Heisig-Gunkel and
Gunkel, 1982). Fish tissue samples obtained from brook trout, blue-
gills, and fathead minnows after chronic exposure contained residues
below detectable limits (Macek et al., 1976). A study of the bio-
accumulation mechanism in whitefish, which were found to have a
bioconcentration factor of 2-3, showed that the herbicide concen-
tration in the water and in the organism reached equilibrium as a
result of the fish's atrazine uptake and simultaneous atrazine
14
-------
secretion (Gunkel and Streit, 1980; Gunkel, 1981). Aquatic plants,
however, may bioaccumulate atrazine. The alga, Chlorella, was found
to have a bioaccumulation factor of 52 based on wet weight. Diatoms
bioaccumulated labeled atrazine 50-100 times (activity-unit volume
algae/activity-unit volume water). This value, however, may be
smaller because activity of capillary water in the algal sample would
decrease the activity of the actual sample. Bioconcentration of
atrazine in diatoms on a dry-weight basis is approximately 150-300
times (Streit, 1979). Additional experiments with diatoms, limpets,
and leeches indicated that food-chain magnification is not significant
(Streit, 1979).
Health Effects
Mammalian toxicity of atrazine is low (Patty, 1981). Oral acute
LD50 (median lethal dose) values for rats and mice ranged from 1400 to
3080 mg/kg (Table 2).
Toxicity of atrazine varied with route of exposure. Atrazine was
more acutely toxic in rats after interperitoneal injection (LD50 125
mg/kg) (Gzhetotskii et al., 1977). Dermal exposure, however, was less
toxic. A dermal LD50 value of 7500 mg/kg was obtained for rabbits
(Patty, 1981). Inhalation studies with rats found no effects after 1-
hr exposure to aerosol concentrations ranging from 1.8 to 4.9 mg/L of
atmosphere, which was the highest concentration tested (WSSA, 1976).
A threshold limit value (TLV) of 10 mg/m3 (8-hr time-weighted average)
has been recommended and is based on low mammalian toxicity and rapid
elimination from animals (Patty, 1981). This TVL value is usually
assigned to nuisance particulates. Generally, the Atrazines are con-
sidered, at most, mild skin and eye irritants (Patty, 1981). Dermal
application of 2800 mg/kg to rats caused a local skin reaction
(Gzhetotskii et al., 1977).
Information on chronic studies is limited. A no-observed-effect
level (NOEL) of 100 ppm was obtained for rats after 2 years of oral
exposure (WSSA, 1979). In contrast, chronic exposure of 0.1 mg/kg to
rats caused increased permeability of blood vessels and leukolyte
count, and decreases in hemoglobin. Changes also included pericapil-
lary and capillary edemas in the brain, swelling or corrugation of
Purkinje cells in the cerebellum, decreased development of gametes in
the ovary and one case of slight perivascular infiltration on the
kidney. Another study also found that atrazine at 10 or 50 mg/kg/day
administered orally to rats for 6 months inhibited growth, caused
luekopenia and affected metabolism of thiamine and riboflavin (Patty,
1981). A higher dose in the same study, 20 mg/kg, caused severe
morphological alterations of the central nervous system and the
parenchymal, endocrine, secretory, and sexual organs. Death occurred
in 40% of the animals with symptoms such as respiratory distress and
paralysis of limbs. Because no information on experimental metho-
dology was available, the two studies cannot be evaluated further
(Nezefi, 1971).
15
-------
UJ
z
cc
*
u.
o
3
>
UJ
Q£
UJ
h-
CC
UJ
H-
_J
t/)
0
UJ
u.
Lu
UJ
J
S
u.
o
i
CM
UJ
1
00
Ol
u
c
fc.
Ol
Ol
ce
liscellaneous
Observed
Effects
c
0
Ol ""
>l U 4->
"3 U
3 l/)
Q.
C c e
tJ i; E
5? «^»
.g Q -0
3 Q. QJ
cS5*
*/» 4->
Qj *O
t- u
^*
01
_l
£
3
n.
X
UJ
VI
Ol
jjj
D.
I/)
4_)
Ol
h
~* "~ ^* *-* -^ r«* i i «^ f*» ^»
00 " Ol Oi CO * o» CO * O» Ol
t < VI Ol t ' V) f-t t/1
*J ^4 4J« *J . .
O^j O - o -^
4_} 4) to ^C 4^ O) ^3 4~* 01 *O 01
'O N4-»COfO NJ4-> 'Otsl^OI
Cu UOJ^Cu C3OI CUCJ3O13C
T3
Ol 1
^ U »*- VI O
Ol T3 ^3 f~ O *O v*
VOIOI Ol IC*O OIOI3
3 4-> C * >) Ok Jrf t--OOl>>
>>IOU O 1- T3 4-1 D E Vl»» O O U.
lt»**»l.U'O 4-> 4^ '"^O ^ VI <^
cn*j 4J c * vi ^o , o 01 o. « eo viooi *
o e i»- »- ^ocvi-o»-o>> o) E CM 3 wuie
^^l-'OO> VI O Q) C3J= kfl) <0>>0 l-
Ol Ol i c c
0 01 C 0 -0 01 0) O <0 * X-O J< 3
U*>4->O>~-.0 O)U1.VIE«M VIJZO) ^x.j3vlO
o. o - > x ex 01 « u in
i- js o j3 w L.aia>ai*OE3 -o i- E9>ai ">
o -~ M cu E
£34^13 vit/) U4^4^^vi u**~vi *-*Cv>4-»aj
ocvuc ^z>«oi«« ex o E js oi 01 >,-o
^H-«-^«-E .*J *J ID O S- *J u. OVO
333J3E >^3 JT U
U O O 3 (J /"
4 < «C LO VD C\J ^ i t O "^*
CTt
^ 0) CTt ^
"-*. -« ^ Oi *^
* ~? *% g. i | f
go. ex E o>
o p
f^ co CD m co ID ^^
-< o <» CM o CM .
i « ro
O O O 1 I O O
\n \f> in LU ui in ID
o o a Q o O u
_i i _i se 2 _i ±i
Ol
Z tt
£ c
E O
3 .
§ ?!
. s|f
VI 3 C o
e? 88£
^ c 01
10 -^ US
4J "O 4J Ol
Ol Ol Ol >
_i -a i- i.
L. Ol
go c vi
U » J3
Ol O
o i. -o
o
II Z H 11
g" gcJ
sgi^i
^< CM ro w
16
-------
^
UJ
=)
z
t
z
o
CM
UJ
CD
2
01
U
C
£
Ol
OJ
C£
!
Miscellaneot
Observed
Effects
c
o
01 -
>, U 4->
IO O
k. -
O" i/i y
O.
IO
o ^
S ^
OJ >" "
3 g"^
C
O
4-J -
I/I 4-1
£ 2
<§
01
Ol
^
o
o.
X
UJ
I/I
Ol
u
CO
AJ
Ol
(
o
o
(J
o
ii
I/I
t-
Ol <*)
OJ Ol
O- -J
i/i "u i-
S- C OJ
.- 1C 4J
W 4iJ E * **"
> L. JC fc. ~~
OJ Ol O O I"
*O fO l» L. O. Ol
Ol IO L) *lfe *"
I/I ^ CX Ol I/I OJ
3 *e oj i- 4-> c
OlO CO o
.*- - Ol C
~-» O l^ 4- H. IO
§§.5 o 3 -s $
I- 'OX
O Q it- C Ol O I.
csj g o oi i« z o
u
c
0
u
Ul t^
"o I
4J "c
5«r
8
L
O
U 1
C 10
C l/l
Ol Ol
O) Ol
Q.4J
** O
0 JT
Ol
Z|j
£ 5 li
Ol
^^
Ol
E
1
ri
i
10
cc
"o
o
^
c
i/i
Ol (*»
o> en
a. i
i.
OJ
.4
s
effect on Ipup
weaning weight
Z'c
u
§
(J
* t/1
II
o
CJ W
tfl
3
O
£§
*J *J
U QJ
-§?
I/I
U 1
C IO
C VI
Ol OJ
OJ Ol
Q.4J
Ol
i 3
^*i ^ O
4O JS *^
0 4-1 4J
Ol
fc>
i1
§
CXJ
_J
UJ
i
£
o**
I 1
o^ *
r^ c
r~* i-
. 1
1/1 I/I
I/) IO
3 CD
>,
1 4->
o --
1- U ^ >
f*S *^ ^) .^
H5 O)-^ U J3
UJ3 10
O 3 "- OJ
Ol JC 01 3
l/i "O C l/l irt
3 *- *- * i/l
m 4j i. *-
L) E ^ Ol 4J
B C 4J
cn 10 w c
J« -O OJ
-*. o» * C (
01 u u *- u m
C OJ J3 ro
3 «- O 1
o »- x: co
o c ai u e>j
£ i
i. i.
o o
u
c
o
s-
jr 01
U 4>J
JD 3
3 U
§.
in
PJ
_t
LU
*
O
o
CT> CO
» °^
._(
/ *
< 2
t^ IO
X 0-
J=
o. u
o - c
oil
(o 01 vn
L. 1 4->
Ol ui <0
«/l I/I C 4-> 4-»
SO) »- C -
t. IO I.
Ol^ Kl ^
JX 0 i. f-
*^. O !- IO
^S E -o ~
-4 E C
z" £ 8 £ .1 9>
fMV
IO
p E C
10 10 10 C ai *
t. i. i- a> >i -v
O O O Q UJ CO
_u _o
c c
£ B
oi JT j=
4J O U
S 3 i o: a «
< l/> l/> Z S S
01
JK
Ol
& a. o
in in in
evj tsj rv
UJ UJ S
Q D O
OJ 4->
f- O) -^
4J I/I J3
10 100*0
u tj z ce
-------
01
u
Ol
01
O£
scellaneous
Observed
Effects
c
Sc
o
VI t/l
c c
C J=
m <-3
<«- O <"> c Q. C 3
**- O O "O X *0 *J
Ol f-N tn oi 0) O)
>» *U-
- "D JC
01 E
'Di.
O
c:
10
OJ
C U3
0 CM
o cr»
>- « t
3 a>«
T3 Olin-^ l."O
OJ J2 Ol
XI- » C "-
>-*-* O O) O» O» t.
D
Z
c
o
OJ *
I U <->
C 10
10 3 W
3 VI
o- vi o
< £
O.
VI JJ
a> >o
JT O U *J ro QJ
i- vi jc i. o
>.*-> >i 3 Oi J= >,
*O U "O
"D 3 "O
^.D -^
C7> O C7>
- -
^ a.*-** F o 01*^13 *o
O*OJ O^*OUDJC O> O) U
E I- E *-> *J o o
\- -a ceo
incoocu-oo>s
Ol O
o.
4^
in re
i-
10 +J
Jg
c u
re c
c
vc u
.. OJ
(U X
QJ U.
C *-
c X
O 10
T3
5 xi oi
»-«*- C -*J
4J O X >O 3 V>
fo .a c oi
4-> O. 3
Ol C "O 3 E *~
J- 3 Ol O T
O E O f>
o re i c oi
toi -^ *>
VI JS 3
S3 3 C
4-> L. "-
u o> JT E
t- C C O> T
>t- 01 -r- -r- 0
- ft) N JZ J3 m
c S 10
cn*J t. oi Oi T!
- oi *J jr j= c
I/I JD fO *J J-» 10
» fo
VI L.
01 t. J-> -O
r Ol *O Ol
ti- jr vi
Ol
X C fc
§in » C
in x "O
a . -o oi "»-
C 3 C
10 n- *J - in
a; o vi i^ * i
t T; vi
J= Ol O>
O *J ^
c -o 3
VI 3
at c u
vi O
IO «- Ol VI
ai *j *J oi
C co X
u u o D.
£.55 I
JD Ou vi
o * E
"- X'O
O Ol O
**- E o
I O C-
*r vi - ^
VI -O
c o>
o jr
vi ij
l_ ^j
4) T3
Q. E
^O >s
^^
V» OJ tfl
O (^
d O 0
X ^" U
Q; u *j
c
C\J VC O
^ I U
O
O f i-
CM *> Q
O N .C O N O. >
n c ic t-
.
§-u *-> > 4-1
<8 M "- "O
- o o c
O C
c
i
O u in
) -D O 4-> T5
Tv.ro f c in wi
c en u ai C-D 01
~-
-a LU oi o> v>
CO O O > "^ jc o
I V i. It. 01 C. C -i-
«3<i Q-O-O'f-ja
c
O VI
r- Ol
<-> -a
10
u u
a. i.
5-5
O CVJ
c x?
O vi c
o. oi oi E
< j=~ n IM
.
O 01
JJ 1-
c u
o «
t_' u
us »
a> a.
s- o
Ol ^>
CX*J
Oi Ol
s
o
a.
X
01
c 3 a.
t -a vi
3 c o
X oi <
^
> en c
= o
O VI
1/-I
LU
§
a.
Ol
a
j=
to
r E
u vi ai
v» ^ u
-------
o
LU
O
£
- *^
Ist
^
c
o
QJ
>! O 4->
4-> C 10
"- 10 O
I. "-
31/1
*f GJ
0.
l/l
0 j,
" = _=
5 o -5
3 g-^
Q£
i/> *J
O) *«
h- U
i?
"QJ
Ol
_j
OJ
3
S
Q.
X
LU
t/t
QJ
O.
UO
in
,2
1/1 r »-
Z CO
O -f- CTi QJ QJ
C "U « '
*o o o
0 C C
J* 4J . OJ QJ
- U * 'I- -
C r^ QJ 10 l. o &. C
V. f^ CD O.CO O.C
3 O"< QJ 4-» o o^ o <
Zi OOlJi 1 -Jr
fO
1 C £
x c -o * c *J
QJ O C O QJ
I/I IO fl QJ ^ QJ QJ
JT 4-1 O 4-1 C I C
QJ4^OOJCOOIOIE *-* OJ
IB i»- QJIO i*- oji/i'^^o i/iE4-J ^o. WEO*^-
O> Ol ^ ^J ^L O ^^ O 41* ^ ***-
4-IQJ O^"4J4^ O E 'B U^- ^W !*-!*- -i- E
Co -'oo coj '^"u iC4-»c I'O'oc tree i^*j 11
O QJ It-EC «E It- QJ 1 O Q) O 1 CO 1 O 1 O 1
Ol. O 3 OO * J* Ol E - OICIO"- OJC-^ QJ C * ft)i
^ C I/I **") *^l/l CC >l/l 4^ >O 4J >O4-> >O >l
§tn vt- O O1-- V C «9 C "O f--^lO ^- c -~
^ CO 4/11 » (OIO'^'^ *f 1C *^ ^O*O>^ *O
C71C UC (7)^- X CTCl~4>J ^I4J^4-* (/I4J4J Ol4^^ Ol
* o ^ O *^ r* OQJ QjOWo 013*00 O3O OI3*O Ol
i/^ ^*- !c o c oo o z t/i z o E ^3 Z E E *o *^ E *o «c E E ^E
I/I I/I
0 0
i. <-
4J 4J
c c
o o ee QJ gt K
0
I-
tj
1 QJ
ra c
O Ol
c »«
>« (Si
-* -O -H
O OJ C
. Ol
OH- O
QJ
o
1
I/I V. VI
>- 1- QJ *o Ol
p oi o j: o
i 10 O ' i~ ) *0 O '*
ZJTO1 L. I/I O>3 I/I * »
ujao 10"- ce o «o-'
ooc jc> O1^ ham .c:
^1/1*0 001 EC '''-fi w
h-o 01- -=0. J=S o
O 5 QJ lOQJ !O>i O Ol *v
ZTQE LOU l/)4->l'^>Qj «"
3
D
n
H
i
U 4->
u c
S Q.
§0 e
C 0
- «
A 4->
L. e IB
: *-
>
j
J
19
-------
c
Ol
1-
0)
1*.
OJ
Miscellaneous
Observed
Effects
c
o
01
>i O *->
4J C 10
IO O
I.
Cr in o
< *
o.
C Q,
*o ^ ^
3 3
«! o^
3 g"^
et ^
^ g
l/l 4J
a; 10
^ L.
3
O
I
in
O
Q.
X
UJ
in
OJ
Q.
to
£
a) «
o
o c
c , 10 a
OJ ' -
1 T^ X 4.
O.CO Ol C
O Cft i C
1 -H a. ti
0-0 c
4^ QJ OCQJiOOJC-C
c i i- i i- o E 6OU4-
^ E 3 aj 3QJ'^OC1. Q *» »
L.Q. L-EO 0)t*-C OJU.IO QL- OL.f A^
i^i*- i*.i^.-^- 3 3inio u u |Q Ei>
1 ID C 1 10 *J IOJ->- F C"5 D4JU D*J« D-^"- 4)^-iO OJ C
>O4-> >o > c 10 > c > *j *j > *j >c
10 z ,
o
kD
t
I
k. QJ l-
01 C I. O
'S E *
E in > u
10 en oi >i <
c. f-. <- c c i1 (
;, O) D O 5
aj u c j3 i. i
in "- 10
aj m c >~ aj in ^ ;
C ^- ^ */* ^~ u
(J U X UJ Z U I/}
^-t
c
> C»
1C OJ
IO -
X 4-1
: oi c
iZ 15
o
a) u-
4J in o
C 3
IB I- IB L.
: a) o D
» c. u *J e -a
^- l»- « O L.
I I. C 10 C-^ O
o a; c in
: en c o N L. c
>ft)
C 3 I/I IB 4«* 0) >>
. i o EL.> * 10 i. J2
) nj i o) E i
. ic i > 4J fi. i -o >> aj
: 01 a>cucx O) a; o T:
> c *-> >OIB >mc3
Jv-o -*-O in ^-iBfl)4J
;mt.
j *J 0
: c i CL
L s:si
aj
|
^
O
T)
H
in
C
V IB
0 (-
in 01
c ^=
> el u
i! «F
u a)|o
J Mia.
)
X
s
c
o>
*o
o.
1
1
0)
O. (O
£
§
<_)
«
in
4J 10
O f
'o.'cn
^j*
^3
13
u. rr>
i
IO
01
20
-------
o
LJ
zr
o
^.
f
CV
, , )
I
l»
OJ
u
c
OJ
i-
OJ
OJ
l/l
IV ? U
i
c
0
OJ
>> O 4->
4J e
C^ 1/1 u
OJ
O
O!
c.
in
4J
fl
OJ
t
OOOOO O O o
co m co co co co co co
^-< »-l « 1 ^* f^ ^H P-H ^H
* ..< /*
i- 1- 1- I- 1- u 1- u
OJOJOJOlOJ Ol Ol OJ
C TT T5 T) T3 TJ "O "O
-O 4-> C
4JC7) 4^4J«O 4^ 4->C 3t 4^ OJ
Cl^J^ C« C C«>> E4J CC l^~ Cnr
.^^rjl -a-- ^OJ' TJ" "O » e > T)?O -D " 13IOE O
\ E i- o--" i- e en u Q. uexo>n s- E -c i- o.4J i. E ^
^ ^5 *O O *O 1 Jtf *O *O *" *O (O (O *O X&-*^ o^
>nO L.OJ L.c/)C7l UOI L.OJ'O'^ L. * ' C*O L.O)<^~ UO>I 4->V
OJ O O 4J ^"*- OOE O4-* O4-f>OJ ^~" O *O in ^^- O ** 4J o ** m *^
i c« c i « E i o i *o c i 10 4j i
>CXOJ4-> > O > O > O 4J > O OJ E > Q.4J OJ E >OZ > O 4-> >
M- 4J fO »- -f- CNJ »- *- *- H- (O »- ^ ^«s E -^- (O4^ ^^^ '^^-C'O »-
a ai .S .^ (oiou-i -f-mm H-«O"- -^io^4j§ oi -^ § «> o * ,
L, U O (/>
o oj o o .c *
O)
o
"o i- j^J
o *d »/* 4*
c l/> JE OJ U
«§«0 30 01- i
_.;: f o >iO « E
t- t. U ^Ulro EI 5-
01 O C if O O ±
c 1 i- afeo -wo oj 5-
§.I OJ b. M OJ Q 0 J~
e.cf OIS'^JSI Ol^^ ^
£ a. o CITS ^5 i- OJ c^ y.
IO>> t/1 Irt'^OO 4JO P"* "
l/> w| UJ ^
-> c
: o
4J
a.
L. -^
11 4-1
W O
>- "0
>o
2^
1 O
U <-l
u t
> in
§,
cO
-j
^
^
>
j
j
^
21
-------
_
=3
Z
0
ii
E
c
O
Ol
X O 4-1
' TO u
I I. M-
3
X
LJ
1
O.
I/O
i/>
2
o
CO
en
« i
^
01
O
5
L.
01
O 4-1
.f- <4_ C
4J >
1 O *
1 4-*
01 Ol U
> c n
4-> t/1 *J
we
o t.
CL u 0.
5
vi
3
F VI
* C
Ol 3
Q.-D
t/l '-
< C
SO O O O O
CO CO 00 CO CO
CT^ C^ C^ CT* C^ Cf^
/
1." > t." 1-* t."
D Ol Ol Ol O>
O "G T3 "O -O -O
5 5 < « 5 S
C 13 i "S
o 01 E c -o
a jj-oo-oo 01
oi4J Ec«> E » we £ *J ie
> O1^ 3O1O u *O 4-***- - *
ff «^ g t/i ^ * (/t flj ^^» IQ ^j -^ 1 3* C ^3 O^
IA*C oa.-*^ QEOI oi**--*-> i- *- (oai.^
i^ a; O E u E i -* f«a 41 4J 4-> CE"^
utic ow-X^ uj= sino Ti "o.^- tD o O
i o "5 i 10 E i o lain i z ijco
i £ i i "O i £ i >f E i in
01 m oio>o aioirsj ai4-* ^^ a> a> o QJ **^
-,"""' i !?'? ^ S" -2 >₯ -^ ?"? 2i^^'
'!o5-o> "S'ScC ti'ie-o' £ "" o '-o5cG ^.cJc1
Qj ^ tfl Qj L. ^H O t- t/1 O Z PO ftj X *M O OJ ^
Z 2 Z Si
'o o
01 01
~ ~
"o "o
c c
..
iO "0
i_ i-
0 0
D
-0 o C
1» i Q.
A Ol E 01 01
o u u u 01
t/\ Qj Wl
O O C UJ Q 3
i- S o => S o
O O CO LU (J E
22
-------
Atrazine was found to have no effect on reproduction in rats when
administered in the diet but was embryotoxic when administered through
subcutaneous injection. Atrazine administered in the diet from Day 1
of pregnancy throughout gestation had no effect on reproduction at
1000 mg/kg (Peters and Cook, 1973). Atrazine administered through
subcutaneous injection on Days 3, 6, and 9 of gestation had no effect
on reproduction at 200 mg/kg, however, higher concentrations of 800 to
2000 mg/kg were embryotoxic. Another study indicated that long-term
exposure to rats and mice revealed no teratogenic effects, however, no
information on experimental methodology was available (Patty, 1981).
Reproduction in sheep was not affected at 15 mg/kg/day, however, a
higher concentration (30 mg/kg/day) caused 100% mortality of adults
during Days 36 and 60 of gestation. One of the ewes failed to con-
ceive, three had experienced embryo death, and two carried normal
fetuses (Binns and Johnson, 1970).
Atrazine caused mutagenic responses in certain plant and animal
systems. Atrazine alone or atrazine following mammalian activation
was usually nonmutagenic. Atrazine following plant activation,
however, had a strong mutagenic effect. Plewa and Gentile (1976)
suggested that atrazine may be degraded by the plant into environ-
mental mutagenic agents, and a mutagenic metabolite in the environment
could adversely affect human health. Additional concern exists
because atrazine as a plant activated promutagen is not only a
laboratory phenomenon but can occur in the environment at
concentration levels used in modern agricultural practice (Plewa et
al., 1984). Atrazine following plant activation caused a positive
effect on forward mutation in Schizosac~ charomyces pombe (6 mM),
Aspergillus nidulans, Streptomyces coelicolor (6 mm), and Chinese
hamster cells V79 (3.0 mM); unscheduled DNA synthesis in human cells
EUE line (3.0 mm); chromosome aberration in vivo in mouse bone-
marrow cell; gene conversion in Saccharomyces cerevisiae; reversion
(plants grown in soil with 35.3 mg/pot) and pollen waxy locus assay
(in situ field plots, 3.84 kg/ha) in Zea mays; and mitotic crossing
over in Aspergillus nidulans.
Atrazine has caused mutagenicity in some animal systems. Induction
of dominant lethal mutations in mice spermatids occurred at high
concentrations (1500 ppm). Atrazine administered through larval
feeding (0.01 percent) to Drosophila caused a significant increase in
sex-linked recessive lethal and a significant difference in chromosome
loss in comparison to the controls. Mammalian activation caused a
positive effect on forward mutation in E. co^i. (100 mg/kg).
No original data on carcinogenic effects were obtained; however,
information obtained from Ciba-Geigy Corp. stated that long-term
studies in rats and mice revealed no carcinogenic effects on parents
or progeny. Duration and dose were unspecified (Patty, 1981). Walker
et al. (1979) found that 6 to 8 interperitoneal injections of atrazine
at 120 to 140 mg/kg/day inhibited development of Ehrlich ascites tumor
cells in mice. Walker et al. (1979) also found that atrazine
inhibited de novo purine biosynthesis in vivo.
23
-------
\
Information obtained from epidemiological studies also is limited.
Applicability of these studies in determining effects of atrazine on
human health is reduced because the people examined in these studies
were exposed to several pesticides. Long et al. (1969), however,
found a significant correlation between the amount of atrazine used by
the high-use group and the bilirubin 1-minute and 30-minute values.
It was noted that only a small number of subjects were involved in
this study. Yoder et al. (1973) noted a 4-fold increase in chromosome
aberrations detected in lymphocyte cultures from blood samples of
workers exposed to 2,4-D, amitrole, and atrazine during the peak usage
season.
CRITERIA EVALUATION AND RECOMMENDATIONS
No information was found on current water-quality criteria or
standards.
Aquatic Toxicity
An Aquatic Life Criterion as defined by Stephan et al. (1985)
consists of two concentrations: the Criterion Maximum Concentration
(CMC) and the Criterion Continuous Concentration (CCC). While
toxicity data are not available for eight genera, as required by the
Guidelines, there were sufficient aquatic toxicity data to estimate an
advisory concentration.
The CMC is equal to one-half the Final Acute Value (FAV). The
Final Acute Value using the following equations:
Final Acute Value = eA
where:
A = S( 0.05) + L
L =[ (In GMAV) - S( ( p))] /4)
S2 = ((In GMAV)2) - (( (In GMAVM2/4)
(P) - (( ( P))2/4)
P = Cumulative probability as R/(N+1);
R = Rank from "1" for the lowest to "N" for the highest GMAV.
Genus Mean Acute Values (GMAVs) were selected from the reviewed liter-
ature (Table 1). Values used in calculating the Final Acute Value are
listed in Table 3. Acute toxicity test results from Salvelinus fonti-
nalis (salmonid), Lepomis macrochirus (a recreationally important
species), Pimephales promelas (another family in the phylum Chordata),
Daphnia magna (planktonic crustacean), Gammarus fasciatus (benthic
crustacean), and Chironomus tentans (insect) were used to calculate
the Final Acute Value. Laboratory tests and procedures were accept-
able except for tests with C. tentans. Guidelines for deriving water-
quality criteria require that acute toxicity tests with C. tentans be
started with second or third instar larvae, whereas this test was
started with first instar larvae.
24
-------
TABLE 3. DATA USED FOR CALCULATION OF FINAL ACUTE VALUE
Acute LC50 GMAV
Species
Rank
Daphnia magna
Gammarus faciatus
Chironomus tentans
Salvelinus fontinalis
Pimephales promelas
Lepomis macrochirus
6.9
5.7
0.72
6,
5,
6.9
5.7
0.72
6.3
15.0
>8.0
2
1
3
6
5
0.57
0.29
0.14
0.43
0.86
0.71
Substituting values from Table 3 into the formulae gives an
estimated Final Acute Value for atrazine based on six aquatic
species of 0.34 ppm.
The estimated maximum cocentration for atrazine was calculated by
the equation:
Estimated maximum concentration = Final Acute Value
2,
giving a value of 0.17 ppm.
The Criterion Continuous Concentration (CCC) is equal to the
lowest of the Final Chronic Value, the Final Plant Value, and the
Final Residue Value (unless other data show that a lower value should
be used).
Chronic toxicity test results from P. promelas (fish), D. magna
(invertebrate) and C. tentans (acutely sensitive freshwater animal
species) were used to calculate the Final Chronic Value. The Species
Mean Acute-Chronic Ratio was determined for each species (Table 4).
Because the Species Mean Acute-Chronic Ratio increases as the Species
Mean Acute Value increases, the Final Acute-Chronic Ratio was calcu-
lated as the geometric mean of the acute-chronic ratio for the species
whose Species Mean Acute Values are close to the Final Acute Value.
Therefore, the Final Acute-Chronic Ratio is equivalent to the geo-
metric mean of the Species Mean Acute-Chronic Ratio for C. tentans
(1.24) which is closest to the Final Acute Value (0.34). The
Guidelines, however, suggest the use of an acute-chronic ratio of 2
when the ratio falls below this level because of possible
acclimation of the organism. The Final Chronic Value was calculated
by the equation:
Final Acute Value
Final Chronic Value = Final Acute-Chronic Ratio
25
-------
TABLE 4. DATA USED FOR CALCULATION OF FINAL CHRONIC VALUE
Acute LC50 SMCV Acute-Chronic
Species (ppm) (ppm) Ratio
Daphnia magna 6.9 0.6245 11.0488
Chironomus tentans 0.72 0.5831 1.2348
Pimephales promelas 15.0 1.0392 14.4342
Substituting appropriate values into this equation gave a Final
Chronic Value of 0.17 ppm.
A Final Plant Value was not derived because no 96-hour test with
an alga or acceptable chronic test with an aquatic vascular plant, as
required by the EPA guidelines, was found. A Final Residue Value also
was not determined as no maximum permissible tissue concentrations or
bioconcentration/bioaccumulation factors were found. Nevertheless,
it was noted that plant effects occur at concentrations lower than
0.17 ppm. Specifically, concentrations as low as 0.001 mg/L were
found to significantly inhibit algal growth (O'Kelly and Deason,
1976) .
The Criterion Continuous Concentration (CCC) is equal to the
lowest of the Final Chronic Value, Final Plant Value, and Final
Residue Value. While the Final Plant Value and Final Residue Value
were not derived, an advisory concentration was determined to be
equivalent to the lowest effect level found in algae. The advisory
concentration for atrazine, therefore, is 1 ug/L, based on data from
O'Kelly and Deason (1976).
Additional information on the toxicity of atrazine to aquatic
organisms is still needed to fulfill guideline requirements completely
(Table 5). Acute toxicity tests are needed for aquatic animals from
two different families of insects and from a phylum other than arthro-
pods or chordates.
Test results used in calculating the Final Chronic Value are
acceptable except for acute toxicity tests with C. tentans, where the
results are questionable due to the use of first instar larvae instead
of second and third as required by the guidelines. However, it is
likely that acute and chronic toxicity tests are needed for C. tentans
or another acutely sensitive freshwater animal species.
A 96-hour test conducted with an alga or a chronic test conducted
with an aquatic vascular plant in which the concentration of the test
material was measured and the endpoint was biologically important is
needed (Stephan et al., 1985). Several studies which determined the
effect of atrazine on growth and photosynthesis of algae were found,
however, no studies were based on a 96-hour exposure period. A
chronic study determining the effect of atrazine on growth of aquatic
vascular plants was unacceptable because concentrations of atrazine
used in the experiment were not measured. Toxicity tests with aquatic
26
-------
plant species from two different phyla are recommended as two tests
are required by the EPA guidelines if plants are among the most sensi-
tive aquatic organisms. Current studies show that aquatic plants are
extremely sensitive to atrazine and indicate that at least two
toxicity tests with aquatic plants are needed.
A study on bioaccumulation with a freshwater species also is
needed. Some bioaccumulation data were available but not acceptable
because actual tissue concentrations were not mentioned and tests were
not performed using a North American species.
Health Effects
Limited data on health effects were available but were insuffi-
cient to calculate a water-quality criterion (Table 6). Atrazine
generally had a low mammalian toxicity. Most information on animal
toxicity was based on LD50 values and NOELs obtained from review
articles. Little or no information was given on experimental condi-
tions and methodology. NOELs reported in the available literature are
considered inadequate to calculate a water quality criterion. No-
observed-adversed-effeet levels (NOAEL), and lowest-observed-adverse-
effect levels (LOAEL) from studies that meet EPA guidelines are
needed. Nevertheless, the lowest NOEL for oral ingestion of atrazine
found in this search of the literature was 25 ppm. This value was
noted in a number of studies involving different species, and will be
used to derive an advisory concentration of: 0.025 ppm (25 ppm x 0.001
where 0.001 represents an application factor for adjustment of the value
from test animal data to human use) to protect against human health
effects until better data becomes available. Toxicity studies with
atrazine indicate that the compound is not carcinogenic or teratogenic
and therefore further studies are not recommended. Information on the
mutagenicity of atrazine is more abundant, but additional testing may
be needed. Atrazine alone or atrazine following mammalian activation
was usually nonmutagenic, however, atrazine following plant activation
had a strong mutagenic effect.
27
-------
TABLE 5. DATA REQUIREMENTS FOR CALCULATION OF AQUATIC LIFE
INTERIM CRITERIAATRAZINE
Data Requirements
Aquatic Toxicity
Available Data
Acceptability of
Available Data
Acute Test Results from tests on:
A salmonid (class Osteichthyes) YES
A warm water species commercially YES
or recreationally important
(class Osteichthyes)
Another family in the phylum YES
Chordata (fish, amphibian, etc.)
A planktonic crustacean YES
(cladoceran, copepod, etc.)
Benthic crustacean (ostracod, YES
isopod, scud, crayfish, etc.)
Insect (mayfly, dragonfly, YES
damselfly, stonefly, mosquito, etc.)
Phylum other than Arthropoda/ NO
Chordata (Rotifera, Annelida,
Mollusca)
Another family of insect NO
Acute-chronic ratios with species from
three different families:
One fish YES
One invertebrate YES
Acutely sensitive freshwater YES
animal species
Acceptable test results from a test with:
Freshwater algae YES
YES
YES
YES
YES
YES
QUESTIONABLE
(first instar larvae)
A vascular plant
Bioaccumulation factor with a
freshwater species (if a maximum
permissible tissue concentration
is available)
YES
YES
YES
YES
NO
NO
(no 96-hour test)
NO
(no measurement
of atrazine
concentrations)
NO
(no actual tissue
concentration
no North American
species)
28
-------
TABLE 6. DATA REQUIREMENTS FOR CALCULATION OF HEALTH
INTERIM CRITERIAATRAZINE
Data Requirements Acceptability of
Human Health Effects Available Data Available Data
Nonthreshold:
Carcinogen NO
Tumor incidence tests (Incidence of NA
tumor formation significantly more
than the control for at least one
dose level), or
Data set that gives the highest NA
estimate of carcinogenetic risk, or
Lifetime average exposure tests, or NA
Human epidemiology studies NA
(if available, not required)
Threshold:
Noncarcinogens YES NO
No observed adverse effect level NO
(at least 90-day), or
Lowest observed effect level NO
Lowest observed adverse effect level NO
Acceptable Daily Intake:
Daily water consumption YES YES
(EPA approved)
Daily fish consumption YES YES
(EPA approved)
Bioconcentration factor NO
Nonfish dietary intake YES YES
(EPA approved)
Daily intake by inhalation NO
Threshold Limit Value:
(Based on 8-hour time-weighted YES YES
average concentrations in air)
Inhalation Studies:
Available pharmacokinetic data NO
Measurements of absorption efficiency NO
Comparative excretion data NO
NA = Not applicable.
29
-------
REFERENCES
Alder, I.D. 1980. A review of the coordinated research effort on the
on of test systems for the detection of mutagenic effects, sponsored
by the E.E.C. Mutat. Res 74: 77-93.
Bashmurin, A. F. 1974. Toxicity of atrazine for animals. Sb. Rab.
Leningr. Vet. Inst. 36:5-7. Abstract: 77-0886 Health Aspects of
Pesticides, Vol. 10, No. 1, Jan. 1977.
Binns, W., and A. E. Johnson. 1970. Chronic and teratogenic effects
of 2,4-D(2,4-dichlorophenoxyacetic acid) and atrazine (2-chloro-4-
ethylamino-6-isopropylamino-s-triazine) to sheep. Proc. N. Cent. Weed
Contr. Conf. 25:100.
Birge, W. J., J. A. Black, A. G. Westerman, and B. A. Ramey. 1983.
Fish and amphibian embryos - a model system for evaluating teratogeni-
city. Fund. Appl. Toxicol. 3: 237-242.
Cunningham, J. J., W. M. Kemp, M. R. Lewis, and U. C. Stevenson.
1984. Temporal responses of the macrophyte, Potamogeton perfoliatus
L. , and its associated autotrophic community to atrazine exposure in
estuarine microcosms. Estuaries 7 (4B) : 519-530.
Davies, R. P., and A. J. Dobbs. 1984. The prediction of biocon-
centration in fish. Water Res. 18(10): 1253-1262.
DeBertoldi, M., R. Barale, and M. Giovannetti. 1978. Mutagenicity of
pesticides evaluated by means of gene conversion in S_. cerevisiae and
h- IL-k^-Hl^ns. Mutat. Res. 53(2): 174-175.
deNoyelles, F., W. D. Kettle, and D. E. Sinn. 1982. The responses of
plankton communities in experimental ponds to atrazine, the most
heavily used pesticide in the United States. Ecology 63(5): 1285-
1293.
Edwards, C. A. 1975. Persistent pesticides in the environment.
Ed., CRC Press, Cleveland, 177 p.
2nd
Forney, D. R., and D. E. Davis. 1981. Effects of low concentrations
of herbicides on submerged aquatic plants. Weed Sci. 29(6):677-685.
Foster, T. S., and S. V. Khan. 1976. Metabolism of atrazine by the
chicken. J. Agric. Food Chem. 24(3): 566-570.
Frear, D.E.H., and J. E. Boyd. 1967. Use of Daphnj.a magna for the
microbioassay of pesticides. I. Development of standardized techni-
ques for rearing Daphnia and preparation of dosage-mortality curves
for pesticides. J. Econ. Entom. 60(5): 1228-1236.
30
-------
Geyer, H., G. Politzki, and D. Freitag. 1984. Prediction of ecotoxi-
cological behavior of chemicals: relationship between n-octanol/water
partition coefficient and bioaccumulation of organic chemicals by alga
Chiorella. Chemosphere 13(2): 269-284.
Gunkel, G. 1981. Bioaccumulation of a herbicide (atrazine, s-tri-
azine) in the whitefish (Coregonus fera J.).. Uptake and distribution
of the residue in fish. Arch. Hydrobiol. Suppl. 59(2/3): 252-287.
Gunkel, G., and B. Streit. 1980. Mechanisms of bioaccumulation of a
herbicide (atrazine, s-triazine) in a freshwater mollusc (Ancylus
f luviatilis Mull.) and a fish (Coregonus fera Jurine). Water Res. 14:
1573-1584.
Gzhetotskii, M. I., L. V. Shkliaruk, and L. A. Dychok. 1977. Toxico-
logical characteristics of the herbicide zeazin. Vrach. Delo 5: 133-
136. Abstract: 77-2826 Health Aspects of Pesticides Vol. 10, No. 1,
Jan. 1977.
Heisig-Gunkel, G., and G. Gunkel. 1982. Distribution of a herbicide
(atrazine, s-triazine) in Daphnia magna; A new approach to determina-
tion. Arch. Hydrobiol. Suppl. 59(4): 359-376.
Hiltibran, R. C. 1967. Effects of some herbicides on fertilized fish
eggs and fry. Trans. Am. Fish Soc. 96: 414-416.
Jones, T. W., W. M. Kemp, J. C. Stevenson, and J. C. Means. 1982.
Degradation of atrazine in estuarine water/sediment systems and soils.
J. Environ. Qual., 11(4): 632-638.
Jones, T. W., and L. Winchell. 1984. Uptake and photosynthetic
inhibition by atrazine and its degradation products on four species of
submerged vascular plants. J. Environ. Qual. 13(2):243-247.
Kettle, W. D. 1983. Description and analysis of toxicant-induced
responses of aquatic communities in replicated experimental ponds.
Dissertation Abstracts International, B. 43(8)2437. (Abstract).
Kosinksi, R. J. 1984. The effect of terrestrial herbicides on the
community structure of stream periphyton. Environ. Poll. A.
36(2) :165-189. (Abstract).
Long, K. R., V. B. Beat, A. K. Gombart, R. F. Sheets, H. E. Hamilton,
F. Falaballa, D. P. Bonderman, and U. Y. Choi. 1969. The
epidemiology of pesticides in a rural area. Amer. Ind. Hyg. Ass. J.
30(3): 298-304.
Loprieno, N., R. Barale, L. Mariani, S. Presciuttini, A. M. Rossi, I.
Sbrana, and L. Zaccaro. 1980. Results of mutagenicity tests on the
herbicide atrazine. Mutat. Res. 74(3): 250.
31
-------
Lorz, H. W., S. W. Glenn, R. H. Williams, C. M. Kunkel, L. A. Norris,
and R. R. Loper. 1979. Effects of selected herbicides on smelting of
Coho salmon. U.S. Environmental Protection Agency, Office of Research
and Development, Environmental Research Laboratory, Corvallis, Oregon.
103 p.
Macek, K. J., K. S. Buxton, S. Sauter, S. Gnilka, and J. W. Dean.
1976. Chronic toxicity of atrazine to selected aquatic invertebrates
and fishes. U.S. Environmental Protection Agency Office of Research
and Development, Environmental Research Laboratory, Duluth, MN. 49 p.
McEwen, F. L., and G. R. Stephenson. 1979. The use and significance
of pesticides in the environment. John Wiley & Sons, N.Y., 538 p.
Murnik, M. R., and C. L. Nash. 1977. Mutagenicity of the triazine
herbicides atrazine, cyanide, and simazine in Drosophila melanogaster.
J. Toxicol. Environ. Health 3: 691-697.
Nezefi, T. A. 1971. Morphological alterations in the organs of white
rats during chronic treatment with atrazine. Adravookhr. Turkm.
15(3): 9-12. Abstract: 72-1309 Health Aspects of Pesticides Vol. 5,
No. 1, Jan. 1972.
O'Kelly, U. C., and T. R. Deason. 1976. Degradation of pesticides by
algae. U.S. Environmental Protection Agency. Office of Research and
Development. EPA 600/3-76-022. 42 p.
Patty, 1981-1982. Industrial hygiene and toxicology, 3rd Ed., Vol.
2A, 2B, 2C.
Peters, J. W., and R. M. Cook. 1973. Effects of atrazine on reprodu-
ction in rats. Bull. Environ. Contam. Tox. 9(5): 301-304.
Pimentel, D. 1971. Ecological effects of pesticides on non-target
organisms. U.S. Government Printing Office, Washington, D.C. 220 p.
Plewa, M. J., and J. M. Gentile. 1976. Mutagenicity of atrazine: a
maizemicrobe bioassay. Mutat* Res. 38: 287-292.
Plewa, M. J., E. D. Wagner, G. J. Gentile, and J. M. Gentile. 1984.
An evaluation of the genotoxic properties of herbicides following
plant and animal activation. Mutat. Res. 136: 233-245.
Schrober, U., and W. Lampert. 1977. Effects of sublethal concentra-
tions of the herbicide Atrazin. on growth and reproduction of Daphnia
pj^lex. Bull. Environ. Contam. Toxicol. 17(3) :269-277.
Stephan, C. E., D. I. Mount, D. J. Hansen, J. H. Gentile, G. A.
Chapman, and W. A. Brungs. 1985. Guidelines for deriving numerical
national water-quality criteria for the protection of aquatic orga-
nisms and their uses. U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratories,
Duluth, MN.
32
-------
- I
U.S. Environmental Protection Agency
Region 5, Library (PL-12J)
77 West Jackson Boulevard, 12th Floor
Chicago, IL 60604-3590
-------
Stratton, G. W. 1981. The effects of selected pesticides and their
degradation products on microorganisms and Daphnia magna. Disserta-
tion Abstracts International, B. 42(3) :921-922.
Stratton, G. W. 1984. Effects of the herbicide atrazine and its
degradation products, alone and in combination, on phototropic micro-
organisms. Arch. Environ. Contam. Toxicol. 13: 35-42.
Streit, B. 1979. Uptake, accumulation, and release of organic pesti-
cides by benthic invertebrates. Arch. Hydrobiol./Suppl. 55(3/4):
373-400.
Streit, B., and H. M. Peters. 1978. Long-term effects of atrazine to
selected freshwater invertebrates. Arch. Hydrobiol. /Suppl. 55(1):
62-77.
U.S. Fish and Wildlife Service. 1981. Fisheries and Wildlife
Research 1980. 201 p.
Veber, K., J. Zahradnik, I. Breyl, and F. Kredl. 1981. Toxic effect
and accumulation of atrazine in algae. Bull. Environ. Contam.
Toxicol. 27: 872-876.
Walker, C. R. 1964. Simazine and other s-triazines as aquatic herbi-
cides in fish habitats. Weeds 12:134-139.
Walker, E. M., Jr., G. R. Gale, L. M. Atkins, and R. H. Gadsden.
1979. Some effects of atrazine on Ehrlich ascites tumor cells in
vitro and in vivo. Bull. Environ. Contam. Tox. 22:95-102.
WSSA. 1979. Herbicide handbook of the Weed Science Society of
America. 4th Ed., Humphrey Press Inc., Geneva, N.Y. 293 p.
Yoder, J., M. Watson, and W. W. Benson. 1973. Lymphocyte chromosome
analysis of agricultural workers during extensive occupational
exposure to pesticides. Mutat. Res. 21: 335-340.
33
-------